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Biomedical subjects

N Taira

Publications and source records attributed to N Taira.

At least 217 records · Page 12Linked to original sources
PubMed1980

Differential effects of nitroglycerin, trimetazidine, verapamil and SK&F 24260 on venous return as revealed by the open-loop method in the dog.

To obtain detailed information concerning the effects of different vasodilators on venous return, experiments were carried out on 28 dogs by the use of the open-loop method. Blood from the superior and inferior venae cavae was drained at the level of the tricuspid valve into a reservoir, from which blood was pumped into the right atrium at a constant flow rate. Changes in reservoir volume reflected a total blood shift from the experimental dog and indicated changes in venous return. Drugs were administered into the ascending aorta. Nitroglycerin (1-10 micrograms/kg) decreased systemic blood pressure, total peripheral resistance and venous return but scarcely altered heart rate. Trimetazidine (0.3-3 mg/kg) decreased systemic blood pressure, total peripheral resistance, venous return and heart rate. Verapamil (10-100 micrograms/kg) decreased systemic blood pressure, total peripheral resistance and heart rate, and increased venous return. SK&F 24260 (1-10 micrograms/kg) decreased systemic blood pressure, total peripheral resistance and increased venous return. Only high doses (10-30 micrograms/kg) of SK&F 24260 reduced heart rate. Rigorous measurements of systemic output showed that nitroglycerin (10 micrograms/kg), trimetazidine (3 mg/kg), verapamil (100 micrograms/kg), SK&F 24260 ( 10 micrograms/kg) produced no change in this parameter. SK&F 24260 increased venous return even when sino-aortic baroreceptor reflex was eliminated, ruling out reflex venoconstriction as a possible cause of the increased venous return. The results suggest the following: [1] Vasodilators like SK&F 24260 and verapamil increase venous return by decreasing arterial and/or venous resistance. [2] If the effect which increases venous capacitance prevails over the effect which decreases arterial and/or venous resistance, venous return is reduced as is the case of nitroglycerin and trimetazidine.

Animals↗
PubMed1980

Effects of 2-nicotinamidethyl nitrate (SG-75), a new antianginal drug, on the cyclic AMP phosphodiesterase activity.

The effect of a potent coronary vasodilator, SG-75, on the purified cyclic AMP phosphodiesterase of the bovine heart was compared with that of papaverine. SG-75 inhibited the phosphodiesterase activity in a competitive manner, the IC50 being 10 mM. SG-75 was approximately 300 times less potent than papaverine in inhibiting the phosphodiesterase activity. Thus, it is unlikely that the phosphodiesterase inhibition by SG-75 is involved in its vasodilator action.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1980

Effects of Ouabain on atrioventricular conduction: simultaneous observation in the isolated AV node preparation and the in situ heart of the dog.

Effects of ouabain on atrioventricular (AV) conduction were studied by using the canine excised, blood-perfused AV node preparations. Ouabain was continuously infused either selectively into the AV node artery (I) of systematically i.v. into the pentobarbital-anesthetized (II) and the pithed donor dog. (III). AV conduction in the isolated AV node preparation was interrupted by AV block in the half of I and II and in all of III after prominent prolongation of AV conduction time. In the remaining half of I and II, AV conduction was interrupted by accelerated prematures. The prematures continued to increase. After AV block ventricular rate decreased in the half of I and II and the inherent automaticity was sustained in all of III. PQ interval of the donor dog was interrupted by accelerated prematures in all of II and two thirds of III. In one third of III, AV block was induced. Interrupting doses of ouabain in the isolated AV node preparation of II and III and in the pithed donor dog heart were almost similar, all of which were significantly larger than that in pentobarbital-anesthetized dog heart. It is concluded that ouabain depresses directly AV conduction but this effect was modified by sympathetic nerve activity in the nerve-intact animals and also by inherent characteristics of the AV nodal cells.

Animals↗
PubMed1980

Mechanism of cardiovascular action of trapidil.

In anaesthetized, open-chest dogs N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-alpha]pyrimidine-7-amine (trapidil) in doses of 0.3--3 mg/kg i.v. produced increases in coronary sinus outflow and heart rate and decreases in systemic blood pressure and coronary resistance in a dose-dependent manner. Trapidil produced an increase in myocardial oxygen consumption but virtually no change in coronary arteriovenous oxygen difference. At 1.8 mg/kg i.v. of the drug coronary resistance fell to half of the pre-drug value and coronary sinus outflow almost doubled, and so did myocardial oxygen consumption. In isolated, blood-perfused dog heart preparations, trapidil produced coronary vasodilator and positive inotropic and chronotropic effects. Theophylline produced similar effects. Trapidil was a more positive inotropic than positive chronotropic agent, and so was theophylline but to a lesser degree than trapidil. In producing vasodilator and positive inotropic effects trapidil was about 3 times more effective than theophylline. Trapidil and theophylline inhibited the cyclic AMP phosphodiesterase (PDE) activity in crude extracts prepared from the dog ventricular muscle. In this respect trapidil was nearly 3 times more potent than theophylline. It is suggested that PDE inhibition would be a fundamental mechanism of action of trapidil.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1980

Effects of trapidil on electrical activities of canine ventricular muscle.

The effects of N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-alpha]pyrimidine-7-amine (trapidil) on the electrical activities of canine right ventricular muscle were studied using standard microelectrode techniques. Trapidil (10(-4) and 10(-3) mol/l) increased the plateau amplitude and shortened the duration of the action potential without changing the resting membrane potential and the maximum rate of rise of the action potential. Trapidil (10(-3) mol/l) restored regenerative action potentials (the slow response) in the ventricular muscle depolarized by elevation of extracellular K+ concentrations to 30 mmol/l. The slow response induced by trapidil was not affected by pindolol (10(-7) mol/l) which abolished that elicited by isoprenaline (10(-6) mol/l). These results indicate that the action of trapidil on the cardiac cell membrane is to increase the slow inward current during the action potential independently of stimulation of beta-adrenoceptors. Taken together with the results obtained by previous investigations the present results suggest that the increase in slow inward current during the action potential would be responsible for the positive inotropic effect of trapidil and would probably be related to its inhibitory action on cyclic AMP phosphodiesterase.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1980

[A correlation between k-complex and auditory evoked potential (ARP) during the slow wave sleep (stage 3) in man (author's transl)].

For this study, sleep EEG of eleven healthy adult subjects ranged from 25 to 30 years of age were observed during stage 3 and evoked K-complex and AEP were both concordantly recorded to investigate the correlation between latencies of s-components in the K-complexes and N4-components in the AEPs during stage 3. The results obtained were as follow: (1) Three distinct components of K-complex such as sharp wave, slow wave (s-component) and burst wave of 12-14 c/sec were found almost constantly during stage 3. (2) It can be concluded that the evoked K-complexes (s-components) in the EEG were almost equivalent to the AEPs (N4-components) if both were concordantly recorded time-locked to click stimuli which were presented every 10 sec with 15 decibels during stage 3. (3) S-component of K-complex such as slow wave was attributed to the impulse bombardment of the nucleus reticularis thalami which is a frequency gate following the hypothesis of Scheibel, M.E. and Scheibel, A.B..

Adult↗
PubMed1979

Assessment of the effects of vasoactive intestinal peptide (VIP) on blood flow through and salivation of the dog salivary gland in comparison with those of secretin, glucagon and acetylcholine.

1. The vascular bed of the submandibular gland in situ was perfused with blood through the glandular artery at a constant pressure in anesthetized dogs. All drugs were administered intra-arterially. 2. Vasoactive intestinal peptide (VIP), secretin and acetylcholine produced a dose-dependent increase in blood flow through the artery (vasodilatation) but glucagon was almost ineffective. 3. Dose-blood flow response curves for VIP and secretin were parallel, and VIP was about 100 times as potent as secretin on a molar basis. Dose-blood flow response curves for acetylcholine were flatter than those for VIP and secretin. Acetylcholine was approximately as potent as secretin on a molar basis. 4. No tachyphylaxis developed to the vasodilator action of VIP. 5. The vasodilator responses to VIP and to electrical stimulation of the chordolingual nerve were scarcely modified by (-)-hyoscyamine in doses that fully antagonized the vasodilator response to acetylcholine. 6. VIP, secretin and glucagon were ineffective in eliciting salivary secretion. 7. The possibility that VIP is released from parasympathetic vasodilator nerves and mediates the atropine-resistant vasodilatation in the dog submandibular gland is discussed.

Acetylcholine↗
PubMed1979

Circumstantial evidence for increased potassium conductance of membrane of cardiac muscle by 2-nicotinamidoethyl nitrate (SG-75).

The mechanism of action of 2-nicotinamidoethyl nitrate (SG-75), was investigated by the use of arterially blood-perfused papillary muscle preparations of the dog. All drugs were administered intra-arterially. SG-75 shortened the effective refractory period (ERP) and decreased the rate of automaticity and developed tension of the papillary muscle, whereas verapamil failed to change the ERP despite a decrease in the developed tension. SG-75 in extremely high doses induced ventricular fibrillation. Methacholine produced decreases in the rate of automaticity and developed tension, and the actions were abolished by atropine. The SG-75-induced decreases in two parameters were not modified by atropine. These results indicate that the cardiac action of SG-75 differs from that of calcium-antagonistic vasodilators and it is suggested that the basic mechanism of action of SG-75 involves an increase in potassium conductance in the membrane of cardiac muscle, without mediation through muscarinic receptors.

Animals↗
PubMed1979

A further study on antihypertensive action of beta-adrenoceptor blocking agents in conscious, renal hypertensive dogs.

Experiments were carried out on 7 conscious, renal hypertensive dogs with 7 beta-adrenoceptor blocking agents (atenolol, bunitrolol, bunolol, carteolol, nadolol, sotalol and timolol). Three main conclusions may be made from this study: (1) the stronger the beta-adrenoceptor blocking activity the stronger the antihypertensive action; (2) for the antihypertensive action, very strong beta-adrenoceptor blocking activity was needed; (3) d-carteolol, unlike dl-carteolol, had no antihypertensive effect. Thus, the beta-adrenoceptor blocking action per se is a prerequisite for the antihypertensive effect of the beta-adrenoceptor blocking agents.

Adrenergic beta-Antagonists↗
PubMed1979

Simultaneous assessment of the effects of trimetazidine on the myocardium and coronary vasculature of the dog.

The effects of trimetazidine on the electrical and mechanical activities of the myocardium were investigated in comparison with the effect on the coronary blood flow in blood-perfused preparations excised from dog hearts. In the sinoatrial (SA) node preparation trimetazidine injected into the sinus node artery increased blood flow and depressed SA node automaticity. In the atrioventricular (AV) node preparation trimetazidine injected into the AV node artery or the anterior septal artery increased blood flow and equally prolonged AV conduction time. In the papillary muscle preparation trimetazidine injected into the anterior septal artery increased blood flow and depressed force of contraction. These cardiodepressant actions occurred in the same range of doses of trimetazidine that exerted the vasodilator action. This indicates that trimetazidine has no selective activity on the coronary vasculature alone. Moreover, the vasodilator effect was more short-lived than the cardiodepressant action. Trimetazidine injected into the anterior septal artery affected ventricular bipolar electrograms. This, taken together with the prolongation of AV conduction time obtained with the same route of administration, suggests that the cardiodepressant action of trimetazidine is ascribed to the local anaesthetic or the membrane stabilizing action rather than to the calcium-antagonistic action.

Animals↗
PubMed1979

Antihypertensive effect of Niludipine (Bay a 7168) on conscious renal-hypertensive dogs.

In conscious renal-hypertensive dogs (one kidney Grollman type) oral administration of 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic acid-bis-(2-propoxyethyl)-ester (niludipine, Bay a 7168) (1 and 3 mg/kg) produced a rather prompt fall of blood pressure and an increase in heart rate. With 3 mg/kg p.o. of niludipine a fall of blood pressure was marked at its peak effect attained about 45 min after dosing and lasted about 3 h. Prior administration of propranolol (30 mg/kg p.o.) greatly prevented an increase in heart rate accompanying the fall of blood pressure produced by 3 mg/kg p.o. of niludipine but was of no effect on the antihypertensive action. These results, taken together with previous results indicating niludipine to have a potent coronary vasodilator action, suggest that niludipine will be useful as an antihypertensive drug, especially when hypertension is associated with ischemic heart disease or when the reduction of blood pressure is urgent. Combined use of niludipine with a beta-adrenergic blocking agent is recommended.

Animals↗
PubMed1978

Excitation of autonomic nerves by 4-aminopyridine in the isolated, blood-perfused sino-atrial node preparation of the dog.

4-Aminopyridine injected into the sinus node artery produced a long-lasting decrease in sinus rate preceded by a transient increase. With a large dose, a long-lasting increase in sinus rate was superimposed on the long-lasting decrease phase. The long-lasting decrease and increase in sinus rate were abolished by 1-hyoscyamine and propranolol respectively, and both were reduced by tetrodotoxin. These results can be interpreted as being due to excitation of autonomic nerves by 4-aminopyridine.

Animals↗
PubMed1978

Effects of calcium-antagonistic coronary vasodilators, nifedipine and verapamil, on ventricular automaticity of the dog.

In isolated, blood-perfused canine papillary muscles intra-arterial injection of calcium-antagonistic coronary vasodilators, nifedipine and verapamil, produced a dose-related decrease in force of contraction. The ventricular rate of about 40 beats/min was not significantly changed by nifedipine even in doses which profoundly decreased the force of contraction. Verapamil changed the ventricular rate in a biphasic manner, but the changes remained as small as about 10% of the basal rate in doses which markedly suppressed the force of contraction. Calcium chloride elicited an increase in force of contraction but depressed automaticity. The present results show that in response to nifedipine, verapamil and calcium ions, ventricular automaticity has characteristics different from those of the sinus node.

Animals↗